At menopause blood levels of estradiol (E2) decrease to nearly zero.
I have always told women who are menopausal that giving Estrogen to them after menopause lower’s their risk of Alzheimer’s, decreases their insulin resistance and helps decrease belly fat. There are many studies that prove that testosterone decreases the risk of Alzheimer’s Disease (AD) and delays the timing of AD by 10 years. This is what I have always told women to reassure them about taking estrogen and testosterone after their ovaries stop making both hormones. It is a simple concept that the practice of medicine has made very complex, however this new research article in Nature 3-2022 by Dr Kamoroff, helps support the practice of replacing the hormones that women lose with menopause, estrogen and testosterone, to prevent the diseases of aging including Osteoporosis and Dementia.
Let me explain the response of the female body to our ovaries shrinking and essentially dying, which is what women’s ovaries do when we become menopausal. The ovaries are the primary source of estradiol (young women’s estrogen) and the only secretor of testosterone in women. Other androgens are produced by the adrenal gland, but they do not provide a woman with the benefits of pure testosterone.
At menopause blood levels of estradiol (E2) decrease to nearly zero. Free T (the active form of T), and estradiol also decreases to less than 60 pg/dl from a pre-menopausal range of 60-250 pg/dl. In response to this radical change in a woman’s chemistry, and very low levels of Estradiol and Testosterone, the pituitary raises the FSH and LH production, the hormones that, previous to menopause stimulated the ovaries to make more E2 and T. After menopause the increasing of FSH and LH continues to increase and cause hot flashes and night sweats. These two hormones are only suppressed by a woman replacing Estrogen and or Testosterone (T). When women get E2 and T, it causes the FSH and LH to “relax” and stop sending out high levels, so hot flashes and night sweats stop. If E and T are not replaced, LH and FSH continue to be elevated and these symptoms can continue for life!
This most recent study by Dr. Kamaroff goes one step farther toward what I already know about ERT (estrogen replacement therapy), and just described. The only way to stop the cause of elevated FSH and LH, and hot flashes and night sweats, is the replacement of estrogen and testosterone. Giving enough estrogen to achieve pre-menopausal blood levels of these two hormones is to give higher doses than the FDA approves of. It is our goal to prevent AD, dementia and Osteoporosis my dosing adequate Estradiol and Testosterone in the form of subcuticular pellets. Low dose estradiol is not the way to be healthy after menopause. Women need adequate hormones to shut down the FSH and LH surges and that is the way to prevent several of the diseases of aging.
Simply, this new study links the elevation of FSH and LH to the onset of dementia, Alzheimer’s Disease and Osteoporosis (thinning of bones) after menopause.
But how does FSH and LH cause dementia and Alzheimer’s disease? This study blames the elevation of FSH and LH for causing inflammation and the accumulation of B amyloid on neurons in the brain is a response to inflammation. This accumulation of plaque causes Alzheimer’s Disease (AD). It seems that the recommendation of the American College of OBGYN gives to doctors to limit the dose and the time ERT and HT are given is counterproductive to the health of women’s brains and bones. The result is that most women are given too little estrogen, and therefore are still at moderate risk for AD and Osteoporosis. When we give compounded E2 and T with pellets, the FSH and LH are suppressed to pre-menopausal levels, and therefore it is the best way to prevent hot flashes but also prevent osteoporosis and AD that can develop without a sufficient amount of estrogen. It is in this way that women without ERT or who have low dose estrogen replacement oral, or patch have a higher risk of the diseases of aging, AD and Osteoporosis than those women who are given an adequate dose that provides pre-menopausal blood levels.
A second study reported at the American Heart Association’s Epidemiology, Prevention, Lifestyle & Cardiometabolic Health Conference 2022, also reported that the longer a woman is without estrogen, the higher her risk of developing heart disease and dementia. This is consistent with the first study I cited, that links high LH and FSH to these diseases of aging. This study looked at women who go through menopause early, before 40, who therefore have more years of high LH and FSH, and a longer period of time associated with inadequate estradiol and testosterone. The earlier women experience menopause the higher the incidence of Dementia by 1.3 times the rate of women who went through menopause at the normal time, after age 40. The healthier aging without disease occurred in women who had more exposure to Estradiol and Testosterone, and less exposure to elevated FSH and LH.
The bottom line for both research studies is that estradiol is one of the keys to healthy aging, pivotal to preventing the devastating diseases of aging like Osteoporosis, Heart Disease, and Dementia. Estradiol is a hormone that should NOT be dosed to achieve a minimal blood level, and when it is replaced after menopause with reasonable doses meant to achieve a normal physiologic blood level , this one hormone brings a woman’s body back to homeostasis and can lead to healthy aging without the diseases of aging.
March 22, 2022
Follicle-Stimulating Hormone’s Role in Alzheimer Disease, in Mice
Anthony L. Komaroff, MD, reviewing Xiong J et al. Nature 2022 Mar
Blocking FSH in ovariectomized mice protected against cognitive decline.
The incidence of Alzheimer disease (AD) is particularly high in older women, as are levels of follicle-stimulating hormone (FSH). This observation led investigators to wonder whether blocking the action of FSH might be beneficial. In mouse models of AD, ovariectomy (with its associated sharp rise in FSH level) promptly increases the degree of deposition of both β-amyloid and tau, which are cardinal pathologic features of AD.
Following ovariectomy in mice, the researchers administered a monoclonal antibody that blocked the action of FSH. The antibody reduced deposition of both β-amyloid and tau in the brain and protected against cognitive decline. The mechanism for this effect is that blocking FSH also blocks an enzyme that causes accumulation of both β-amyloid and tau. Further incriminating FSH in AD pathology, deposition of β-amyloid and tau also was reduced by using genetic engineering to knock out receptors for FSH, and deposition was increased by raising levels of FSH. FSH also is produced at low levels in males, and the FSH-blocking antibody also reduced hippocampal and cortical deposition of β-amyloid and tau in males. Experiments showed that two other features of menopause — low estrogen levels and high luteinizing hormone levels — did not explain the AD-like features seen in ovariectomized mice.
Many, but not all, findings in mouse models of AD have been replicated in humans. Blocking FSH also reduced bone loss and visceral fat in mice. Given all these theoretical benefits, one might surmise that trials of FSH blockade in humans will be undertaken.
Study: Early menopause may signal women’s dementia risk
A preliminary study to be presented at the American Heart Association’s Epidemiology, Prevention, Lifestyle & Cardiometabolic Health Conference 2022 found that women who experience menopause before they reach 40 years of age may have a 35% increased risk for dementia later in life. The researchers also found that women who entered menopause before they turned 45 years old were 1.3 times more likely to receive an early dementia diagnosis by the time they reach 65 years of age.
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